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      Maternal diet during pregnancy and adaptive changes in the maternal and fetal pancreas have implications for future metabolic health

      review-article
      1 , 2 , , 3
      Frontiers in Endocrinology
      Frontiers Media S.A.
      nutrition, pregnancy, fetus, pancreas, insulin, programming

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          Abstract

          Fetal and neonatal development is a critical period for the establishment of the future metabolic health and disease risk of an individual. Both maternal undernutrition and overnutrition can result in abnormal fetal organ development resulting in inappropriate birth size, child and adult obesity, and increased risk of Type 2 diabetes and cardiovascular diseases. Inappropriate adaptive changes to the maternal pancreas, placental function, and the development of the fetal pancreas in response to nutritional stress during pregnancy are major contributors to a risk trajectory in the offspring. This interconnected maternal-placental-fetal metabolic axis is driven by endocrine signals in response to the availability of nutritional metabolites and can result in cellular stress and premature aging in fetal tissues and the inappropriate expression of key genes involved in metabolic control as a result of long-lasting epigenetic changes. Such changes result is insufficient pancreatic beta-cell mass and function, reduced insulin sensitivity in target tissues such as liver and white adipose and altered development of hypothalamic satiety centres and in basal glucocorticoid levels. Whilst interventions in the obese mother such as dieting and increased exercise, or treatment with insulin or metformin in mothers who develop gestational diabetes, can improve metabolic control and reduce the risk of a large-for-gestational age infant, their effectiveness in changing the adverse metabolic trajectory in the child is as yet unclear.

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          Most cited references201

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          Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth

          Two follow-up studies were carried out to determine whether lower birthweight is related to the occurrence of syndrome X-Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia. The first study included 407 men born in Hertfordshire, England between 1920 and 1930 whose weights at birth and at 1 year of age had been recorded by health visitors. The second study included 266 men and women born in Preston, UK, between 1935 and 1943 whose size at birth had been measured in detail. The prevalence of syndrome X fell progressively in both men and women, from those who had the lowest to those who had the highest birthweights. Of 64-year-old men whose birthweights were 2.95 kg (6.5 pounds) or less, 22% had syndrome X. Their risk of developing syndrome X was more than 10 times greater than that of men whose birthweights were more than 4.31 kg (9.5 pounds). The association between syndrome X and low birthweight was independent of duration of gestation and of possible confounding variables including cigarette smoking, alcohol consumption and social class currently or at birth. In addition to low birthweight, subjects with syndrome X had small head circumference and low ponderal index at birth, and low weight and below-average dental eruption at 1 year of age. It is concluded that Type 2 diabetes and hypertension have a common origin in sub-optimal development in utero, and that syndrome X should perhaps be re-named "the small-baby syndrome".
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            WEIGHT IN INFANCY AND DEATH FROM ISCHAEMIC HEART DISEASE

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              Beta-cell replication is the primary mechanism subserving the postnatal expansion of beta-cell mass in humans.

              Little is known about the capacity, mechanisms, or timing of growth in beta-cell mass in humans. We sought to establish if the predominant expansion of beta-cell mass in humans occurs in early childhood and if, as in rodents, this coincides with relatively abundant beta-cell replication. We also sought to establish if there is a secondary growth in beta-cell mass coincident with the accelerated somatic growth in adolescence. To address these questions, pancreas volume was determined from abdominal computer tomographies in 135 children aged 4 weeks to 20 years, and morphometric analyses were performed in human pancreatic tissue obtained at autopsy from 46 children aged 2 weeks to 21 years. We report that 1) beta-cell mass expands by severalfold from birth to adulthood, 2) islets grow in size rather than in number during this transition, 3) the relative rate of beta-cell growth is highest in infancy and gradually declines thereafter to adulthood with no secondary accelerated growth phase during adolescence, 4) beta-cell mass (and presumably growth) is highly variable between individuals, and 5) a high rate of beta-cell replication is coincident with the major postnatal expansion of beta-cell mass. These data imply that regulation of beta-cell replication during infancy plays a major role in beta-cell mass in adult humans.
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                Author and article information

                Contributors
                URI : https://loop.frontiersin.org/people/1481481Role: Role: Role:
                Role: Role:
                Journal
                Front Endocrinol (Lausanne)
                Front Endocrinol (Lausanne)
                Front. Endocrinol.
                Frontiers in Endocrinology
                Frontiers Media S.A.
                1664-2392
                23 September 2024
                2024
                : 15
                : 1456629
                Affiliations
                [1] 1 Lawson Health Research Institute, St. Joseph’s Health Care , London, ON, Canada
                [2] 2 Departments of Medicine, Physiology and Pharmacology, Western University , London, ON, Canada
                [3] 3 Oxford Centre for Diabetes, Endocrinology, and Metabolism, Wellcome Centre for Human Genetics, University of Oxford , Oxford, United Kingdom
                Author notes

                Edited by: Lawrence Merle Nelson, Mary Elizabeth Conover Foundation, Inc., United States

                Reviewed by: Chellakkan Selvanesan Blesson, Baylor College of Medicine, United States

                Sumiko Morimoto, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico

                *Correspondence: David J. Hill, david.hill@ 123456lawsonresearch.com
                Article
                10.3389/fendo.2024.1456629
                11456468
                39377073
                55209426-5d39-4210-9726-7044ad52ab11
                Copyright © 2024 Hill and Hill

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 28 June 2024
                : 28 August 2024
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 201, Pages: 15, Words: 8153
                Funding
                The author(s) declare financial support was received for the research, authorship, and/or publication of this article. For cited studies that were carried out by the authors, thanks are extended to the Lawson Foundation for financial support in the form of an endowed research chair to DJH. TGH was the recipient of a Novo Nordisk-Oxford Postdoctoral Fellowship.
                Categories
                Endocrinology
                Review
                Custom metadata
                Developmental Endocrinology

                Endocrinology & Diabetes
                nutrition,pregnancy,fetus,pancreas,insulin,programming
                Endocrinology & Diabetes
                nutrition, pregnancy, fetus, pancreas, insulin, programming

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